The ability of the fetal and neonatal liver to form glucuronide conjugates with endogenous and exogenous metabolites has been shown to be poor.1-3 Accordingly, current theory holds that inadequate hepatic conjugation of bilirubin is the essential, if not the sole, mechanism responsible for the bilirubinemia of physiologic icterus. This view does not take account of the possible role of extrahepatic processes of conjugation in the metabolism of bilirubin, and, by implication, places the burden of forming bilirubin glucuronides entirely on the liver. It implies further that the neonatal liver has an adequate capacity for the excretion of such quantities of bilirubin as it is able to conjugate.
Both premises derive in a large measure from the prevailing concept of the nature of the pigment which accumulates in the body fluids and tissues of the newborn infant. It is more or less explicitly assumed that this pigment is solely or
ZUELZER WW, REISMAN LE, BROWN AK. Studies in Hyperbilirubinemia: III. Separate Metabolic Defects in Premature Infants Reflected in the Partition of Serum Bilirubin. Am J Dis Child. 1961;102(6):815–842. doi:10.1001/archpedi.1961.02080010817005
Artificial Intelligence Resource Center
Customize your JAMA Network experience by selecting one or more topics from the list below.